Evaluation of 64Cu-labeled PET Tracers for Imaging Acute Inflammation and Endogenous Hydrogen Sulfide

• Published in: 대한방사성의약품학회지, 9(2) 2023, 9(2), , pp.81-85
• Main Authors: 서혜연, 유란지, 정재민, 이윤상
• Format: Article
• Language: Korean
• Subjects: 방사선과학
• ISSN: 2384-1583; 2508-3848

Hydrogen sulfide (H2S), recognized as the third gasotransmitter with specific implications for inflammation and hypoxia, exhibits affinity for 64Cu immobilization. This study explores the viability of 64Cu-labeled PET tracers in detecting endogenous H2S. In vitro reactivity experiments involved evaluating the interaction between various concentrations of NaHS and 64Cu-labeled chelators at 37℃ in a shaking incubator. In vivo molecular PET imaging studies were conducted using two distinct mouse models. An acute inflammation model, induced with carrageenan, involved administering 2.22 MBq/100 μL of [64Cu]Cu-ATSM or [64Cu]Cu-Cyclen intravenously 4 hours post-inflammation induction, with subsequent PET imaging in static 5 min mode. For the NaHS implantation model, NaHS dissolved in Matrigel was subcutaneously injected into the right dorsal region of BALB/c mice, followed by intravenous injection of radiotracers (2.22 MBq/100 μL) 1 hour later, and subsequent PET imaging. The optimized labeling condition involved dissolving 10 μg of chelators in ammonium acetate buffer and reacting at 60℃ for 20 minutes. Both [64Cu]Cu-Cyclen and [64Cu]Cu-ATSM reacted with various concentrations of NaHS to form insoluble 64CuS. High uptake of [64Cu]Cu-ATSM and [64Cu]Cu-Cyclen in acute inflammatory lesions in the mouse right footpad and the NaHS implantation model suggests their potential as imaging agents for inflammation and H2S in vivo. In conclusion, optimized [64Cu]Cu-ATSM and [64Cu]Cu-Cyclen labeling conditions for endogenous H2S imaging were established, confirming insoluble 64CuS both in vitro and in vivo. [ 64Cu]Cu-ATSM and [64Cu]Cu-Cyclen hold promise as diagnostic agents targeting endogenous H2S in various diseases associated with inflammation and hypoxia. KCI Citation Count: 0